Immunotoxicology group, Department of Ecology, Institute for Biological Research 'Sinisa Stankovic', University of Belgrade, 142 Bulevar despota Stefana, Belgrade 11000, Serbia.
Institute of Zoology, Faculty of Biology, University of Belgrade, 16 Studentski trg, Belgrade 11000, Serbia.
Biomed Environ Sci. 2019 Jul;32(7):508-519. doi: 10.3967/bes2019.068.
The aim of this study is to investigate the effects of oral cadmium (Cd) ingestion on the pulmonary immune response.
Determination of Cd content in lungs and histopathological evaluation of the tissue was performed in rats following 30-day oral Cd administration (5 and 50 mg/L). Antioxidant enzyme defense (superoxide dismutase and catalase), cell infiltration, and production of tumor necrosis factor (TNF) and interferon (IFN)-γ, as well as the activity of myeloperoxidase (MPO), nitric oxide (NO), and various cytokines [interleukin (IL)-1β, IL-6, IL-10, and IL-17] were investigated.
Cd caused tissue damage and cell infiltration in the lungs, and this damage was more pronounced at higher doses. Cd deposition resulted in lung inflammation characterized by a dose-dependent IL-1β increase in lung homogenates, increased TNF levels at both doses, and IL-6 stimulation at low doses with inhibition observed at higher doses. Cd exerted differential effects on lung leukocytes isolated by enzyme digestion, and these effects were characterized by a lack of change in the production of reactive oxygen and nitrogen species, an inhibition of IL-1β and TNF, and stimulation of MPO and IFN-γ. The higher capacity of Cd-exposed lung cells to respond to the opportunistic pathogen Staphylococcus epidermidis was demonstrated in vitro.
The potential of ingested Cd to exert both proinflammatory and immunosuppressive effects on pulmonary tissue inflammation and immune reactivity highlights the complex immunomodulatory actions of this metal.
本研究旨在探讨口服镉（Cd）摄入对肺部免疫反应的影响。
在大鼠口服 Cd 30 天后（5 和 50mg/L），测定肺中 Cd 含量并对组织进行组织病理学评估。测定抗氧化酶防御（超氧化物歧化酶和过氧化氢酶）、细胞浸润以及肿瘤坏死因子（TNF）和干扰素（IFN）-γ的产生，以及髓过氧化物酶（MPO）、一氧化氮（NO）和各种细胞因子[白细胞介素（IL）-1β、IL-6、IL-10 和 IL-17]的活性。
Cd 导致肺部组织损伤和细胞浸润，高剂量时更为明显。Cd 沉积导致肺部炎症，肺匀浆中 IL-1β 呈剂量依赖性增加，两种剂量下 TNF 水平升高，低剂量时 IL-6 刺激，高剂量时抑制。Cd 对酶消化分离的肺白细胞产生不同的影响，其特征是活性氧和氮物种的产生无变化、IL-1β 和 TNF 抑制以及 MPO 和 IFN-γ 刺激。体外实验表明，暴露于 Cd 的肺细胞对机会性病原体表皮葡萄球菌的反应能力增强。
摄入的 Cd 对肺部组织炎症和免疫反应具有促炎和免疫抑制作用，这突出表明了这种金属的复杂免疫调节作用。
